ArticleTranslational stroke research2018
Inactivation of NSF ATPase Leads to Cathepsin B Release After Transient Cerebral Ischemia.
Article in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Interruption of Endolysosomal Trafficking After Focal Brain Ischemia.Frontiers in molecular neuroscience · 2021Pooled it
- Cystatin B Attenuates Cerebral Ischemia Reperfusion Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Vanillic acid inhibits TGF-β type I receptor to protect bone marrow mesenchymal stem cells from radiation-induced bystander effects.Translational cancer research · 2025Article
- Predictive value of circulating SNHG1/miR-194-5p and carotid ultrasound for the onset of cerebral infarction in patients with transient cerebral ischemia.Frontiers in molecular neuroscience · 2025Article
- The role of autophagy in ischemic brain injury.Autophagy reports · 2025Review
- N-ethylmaleimide-sensitive factor elicits a neuroprotection against ischemic neuronal injury by restoring autophagic/lysosomal dysfunction.Cell death discovery · 2024Article
- Downregulation ofFrontiers in aging neuroscience · 2024Article
- The role of synaptic protein NSF in the development and progression of neurological diseases.Frontiers in neuroscience · 2024Review
- The critical role of the endolysosomal system in cerebral ischemia.Neural regeneration research · 2023Review
- Cathepsin B in programmed cell death machinery: mechanisms of execution and regulatory pathways.Cell death & disease · 2023Review
- Interruption of endolysosomal trafficking leads to stroke brain injury.Experimental neurology · 2021Article
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- CID1067700, a late endosome GTPase Rab7 receptor antagonist, attenuates brain atrophy, improves neurologic deficits and inhibits reactive astrogliosis in rat ischemic stroke.Acta pharmacologica Sinica · 2019Article
- The Protein Modification and Degradation Pathways after Brain Ischemia.Translational stroke research · 2018Article
- Nest-building activity as a reproducible and long-term stroke deficit test in a mouse model of stroke.Brain and behavior · 2018Article
- Effects of Vitamin D3 on the NADPH Oxidase and Matrix Metalloproteinase 9 in an Animal Model of Global Cerebral Ischemia.Oxidative medicine and cellular longevity · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Neurons have extraordinary large cell membrane surface area, thus requiring extremely high levels of intracellular membrane-trafficking activities. Consequently, defects in the membrane-trafficking activities preferentially affect neurons. A critical molecule for controlling the membrane-trafficking activities is the N-ethylmaleimide-sensitive factor (NSF) ATPase. This study is to investigate the cascade of events of NSF ATPase inactivation, resulting in a massive buildup of late endosomes (LEs) and fatal release of cathepsin B (CTSB) after transient cerebral ischemia using the 2-vessel occlusion with hypotension (2VO+Hypotension) global brain ischemia model. Rats were subjected to 20 min of transient cerebral ischemia followed by 0.5, 4, 24, and 72 h of reperfusion. Neuronal histopathology and ultrastructure were examined by the light and electron microscopy, respectively. Western blotting and confocal microscopy were utilized for analyzing the levels, redistribution, and co-localization of Golgi apparatus and endosome or lysosome markers. Transient cerebral ischemia leads to delayed neuronal death that occurs at 48-72 h of reperfusion mainly in hippocampal CA1 and neocortical (Cx) layers 3 and 5 pyramidal neurons. During the delayed period, NSF ATPase is irreversibly trapped into inactive protein aggregates selectively in post-ischemic neurons destined to die. NSF inactivation leads to a massive buildup of Golgi fragments, transport vesicles (TVs) and late endosomes (LEs), and release of the 33 kDa LE type of CTSB, which is followed by delayed neuronal death after transient cerebral ischemia. The results support a novel hypothesis that transient cerebral ischemia leads to NSF inactivation, resulting in a cascade of events of fatal release of CTSB and delayed neuronal death after transient cerebral ischemia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.